Nicardipine

• •Acute hypertension management — perioperative HTN, hypertensive emergency, post-CV surgery
• •Acute aortic dissection (after beta-blocker)
• •Pulmonary hypertension acute management (some evidence)
• •Cerebral vasospasm prophylaxis (subarachnoid hemorrhage — nimodipine PO preferred for cerebral)

Onset 5-15 min IV bolus; 30-60 min infusion to peak. Duration 30-60 min after stopping infusion (longer than nitroglycerin). Hepatic metabolism via CYP3A4 (drug interactions). Half-life 2-4 h with linear kinetics. Active metabolite minimal.

↓SVR → ↓BP via afterload reduction. Reflex tachycardia (modest, usually 5-10 bpm). Minimal effect on contractility, conduction, or HR direct effects. Does NOT cause aortic dissection extension (in contrast to pure vasodilators that drop SVR rapidly without HR control).

• !Hypotension (additive with anesthetics)
• !Reflex tachycardia
• !Headache, flushing (vasodilation)
• !Phlebitis at infusion site (peripheral OK; central preferred for sustained infusion)
• !Nausea/vomiting

• ×Severe aortic stenosis (afterload reduction increases gradient + decreases CPP)
• ×Acute MI with hypotension
• ×Hypersensitivity

• ★PREFERRED FIRST-LINE for intraop HTN in non-cardiac surgery — easier to titrate than nitroprusside (no cyanide), no rebound tachycardia of nitroglycerin, longer duration than esmolol.
• ★Combine with esmolol or labetalol for tachycardia + HTN (ESMOLOL FIRST in dissection — esmolol prevents reflex tachy).
• ★INFUSION PUMP titration: typical adult 5 mg/h start, increase by 2.5 mg/h q5-15 min until target. Once at target, titrate downward as anesthetic stabilizes.
• ★Cerebral effects: causes mild cerebral vasodilation (may raise ICP transiently); use cautiously in elevated ICP — but blood pressure control + cerebral perfusion preservation usually outweighs.
• ★Switch to oral antihypertensive (amlodipine, labetalol PO) before stopping infusion — some patients have rebound HTN.

• Epinephrine

  α1 (vasoconstriction), α2, β1 (inotropy + chronotropy), β2 (bronchodilation, vasodilation in skeletal muscle). Dose-dependent receptor preference: low-dose β-predominant, high-dose α-predominant.

• Norepinephrine

  Strong α1 → vasoconstriction. Mild β1 → modest inotropy. Minimal β2.

• Phenylephrine

  Pure α1 agonist → vasoconstriction. No β activity.

• Dexmedetomidine

  α2 agonist (locus coeruleus) → sedation + analgesia + anxiolysis without significant respiratory depression.

• Vasopressin

  Endogenous nonapeptide hormone. V1 receptor agonist on vascular smooth muscle (Gq → IP3 → Ca²⁺ → vasoconstriction). V2 on renal collecting ducts (Gs → cAMP → aquaporin insertion → water reabsorption). At pressor doses (0.01–0.04 U/min), V1 effects dominate.

• Esmolol

  Selective β1-adrenergic receptor antagonist. Decreases HR, contractility, conduction velocity, and AV node refractoriness. Selectivity for β1 over β2 reduces (does not eliminate) bronchospasm risk vs non-selective beta-blockers.

• Magnesium Sulfate

  Multiple mechanisms: (1) NMDA receptor antagonism (anticonvulsant, analgesic); (2) Voltage-gated calcium channel blockade in vascular + uterine smooth muscle (vasodilation, tocolysis); (3) Decreased ACh release at neuromuscular junction (NMB potentiation); (4) Membrane stabilization (antiarrhythmic, especially torsades).

• Amiodarone

  Multichannel blockade — primarily class III (K+ channel block → prolonged repolarization, increased refractory period), plus class I (Na+ block), class II (β-blocker), class IV (Ca²⁺ block) properties. Treats most supraventricular AND ventricular arrhythmias. Long elimination half-life (weeks–months) limits chronic use.

Browse all classes: /reference/drugs